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    Previous Issues Volume 1, Issue 1 - 2016

    Short CommunicationPDF  

    Behavioural Signs and Neurological Disorders in Dogs and Cats

    Amadei Eleonora1, Cantile Carlo1, Gazzano Angelo1, Mariti Chiara1

    Department of Veterinary Sciences - University of Pisa, Viale delle Piagge 2, 56124 Pisa, Italy.

    CorrespondingAuthor:Mariti Chiara, Department of Veterinary Sciences - University of Pisa, Viale delle Piagge 2, 56124 Pisa, Italy,Tel: 0039-050-2216837; Email: chiara.mariti@unipi.it

    Received Date: 20 Feb 2016 
    Accepted Date: 04 Apr 2016  
    Published Date: 15 Apr 2016

    Copyright © 2016 Mariti C.

    Citation: Mariti C. (2016). Behavioural Signs and Neurological Disorders in Dogs and Cats. Mathews J Vet Sci. 1(1): 001.

     

    INTRODUCTION

    Veterinary behavioural medicine is relatively new, and its evolution may suffer more than other specialties from an unclear identity, because so many disparate groups who are not rooted in veterinary medicine have participated in its evolution [1]. In the past, behavioural problems of companion animals were not dealt by veterinarians, but mainly by dog trainers [2]. When animal clinical psychology started to be developed as a new scientific discipline, the interest increased also in the veterinary field [3]. In 1997 in Birmingham (UK) was held the first International Meeting on veterinary behavioural medicine [4]. Later, the general approach and terminology was more in line with psychiatry than with psychology, and behavioural problems were seen as a trauma or an infection, with a physical cause to be treated in order to solve the problem [5-7]. However, blind adherence to a medical model causes serious problems when it comes to the scientific investigation of problem behaviour. In fact, the use of medical paradigms for the study of problem behaviour which seek to categorise disorders rather than focus on their underlying mechanism and evolutionary function, may restrict the development of our knowledge of these processes [8].
    Behaviour is the ultimate integrator of all organ system responses, and as such, is a dynamic outcome resulting from the interactions of complex mechanisms. Understanding such systems is difficult, but progress can occur if an attempt is made to understand all the mechanistic levels that contribute to behavioural patterns and behavioural conditions [1].
    Historically veterinary medicine has focused on differentiating between behavioural and physical problems; priority was given to the diagnosis and treatment of physical diseases, and only after having dealt with them the behavioural component was taken into account. A more holistic approach is desirable, dealing contemporaneously with physical and behavioural components, in order to optimize the patient’s welfare. This should be particularly true for neurology, as the boundary between a neurological disease and a behavioural problem is often unclear. For instance, all disorders involving the central nervous system, especially the forebrain, have a consequence on behaviour [9].
    A strict collaboration between veterinary neurologists and behaviourists is desirable [10, 11]. Such collaboration would be beneficial for both veterinary neurologists and behaviourists to have a multidisciplinary approach. On one hand neurologists, together with the use of advanced diagnostic methods and the exclusion of metabolic and infectious diseases, may dwell also on the behavioural aspects and taking into account, when needed, the possibility of a behavioural consultation for the animal patient. On the other hand, behaviourists should take into account to perform a complete physical examination, including a neurological examination, on a subject displaying behavioural problems. However, it must be considered that a normal neurological examination does not allow to exclude the presence of neurological problems. For instance, an intracranic neoplasia can result in a normal neurological examination and the only sign, for a long time, can be a change in behaviour [11, 12].
    The challenge is to determine the sensible limit to clinical investigation. Once basic medical data have been obtained (including general physical examination, neurological examination, and blood tests), the level of consistency between a particular pattern of behaviour and the environment within which it is expressed may help to decide whether there is likely to be an underlying medical condition, and whether it may be necessary to perform additional medical tests [13].
    In the scientific literature there are many physical diseases (such as infections, endocrinologic disorders, neoplasia, toxins, congenital lesions, degenerative diseases and allergies) that are recognized to be associated with behavioural signs [5, 13, 14]. As a matter of fact, often owners realize that their animal is ill when the dog or the cat changes the behaviour, even if it is not a behavioural problem and owners refer this behavioural change to the veterinarian [15]. In particular, many neurological disorders can lead to behavioural modifications; and for many abnormal behaviours there is not yet a clear distinction between neurological and behavioural disorder. This is the case of compulsive disorders, some of which can benefit from a treatment with anti-epileptic drugs while others are solved with psychoactive drugs normally used for behavioural problems [11, 16, 17]. In addition, diseases related to perception such as blindness are responsible for clear modifications of the behaviour [18].
    When approaching a differential diagnosis, surgical sieves are commonly used. Using the acronym VITAMIN-D and the available scientific literature, we created a table (Table 1) summarizing a series of behavioural problems and their possible associations with neurological disorders [10, 11, 15, 16, 19-67].

     

    Table 1: Central nervous system diseases based on the VITAMIN-D acronym for dogs and cats. V = vascular, I = inflammatory/infectious, T = trauma, A = anomalous, M = metabolic, I = idiopathic, N = neoplasia, D = degenerative. FIP = feline infectious peritonitis, FIV = feline immunodeficiency virus infection, FSE = feline spongiform encephalopathy; n.r.= not reported.

    POSSIBLE BEHAVIOURAL SIGNS UNDERLYING NEUROLOGICAL CONDITIONS
    Inappropriate elimination/urogenital diseases V: n.r.
    I: Distemper.
    T: Intervertebral disc disease.
    A: Lissencephaly, hydrocephalus, hydrosyringomyelia.
    M: Hepatic encephalopathy, uremic syndrome, hypercalcemia, hyperthyroidism, hyper- or hypoadrenocorticism.
    I: Neurogenic cystitis, idiopathic cystitis.
    N: Neoplasia of the basal nuclei, thalamus, cerebellum, pudendal nerve.
    D: Neurodegenerative conditions of the basal nuclei, thalamus, cerebellum, pudendal nerve; upper and lower motor neuron diseases.
    Aggressive behavior V: Feline ischemic encephalopathy, cerebrovascular accidents, brain hypoxia.
    I: Distemper, cryptococcosis, FSE, FIP, rabies, toxoplasmosis, neosporosis, Borna disease, steroid responsive arteritis-meningitis, Reflex sympathetic dystrophy.
    T: Brain trauma.
    A: Lissencephaly, hydrocephalus, porencephaly.
    M: Hepatic encephalopathy, uremic syndrome, hypercalcemia, hyper- or hypothyroidism, hyper- or hypoadrenocorticism, heavy metal poisoning.
    I: Neurogenic cystitis, idiopathic ganglioradiculoneuritis, feline hyperesthesia syndrome, idiopathic epilepsy.
    N: Intracranial tumors: temporal lobes, limbic system, hypothalamus (ventromedial and posterolateral areas in the cat).
    D: Polioencephalomalacia of the pyriform lobe and hippocampus, lysosomal storage diseases, mitochondrial encephalopathies.
    Depression, reduced activity, somnolence, apathetic behavior V: Feline ischemic encephalopathy, cerebrovascular accidents, brain hypoxia.
    I: Distemper, cryptococcosis, protothecosis, canine erhlichiosis, canine encephalitozoonosis, bacterial meningoencephalitis, necrotizing meningoencephalitis, necrotizing leukoencephalitis, granulomatous meningoencephalomyelitis, steroid responsive arteritis-meningitis, FSE, FIP, FIV, Borna disease.
    T: Brain trauma.
    A: Lissencephaly, hydrocephalus.
    M: Hepatic encephalopathy, uremic syndrome, hypercalcemia, hyper- or hypothyroidism, hyperadrenocorticism, hypoglycemia, heavy metal poisoning, Marijuana poisoning.
    I: n.r.
    N: Intracranial tumors: thalamus, frontal lobes, tegmentum of midbrain and pons.
    D: Lysosomal storage diseases, spongy degeneration of the gray matter, necrotizing encephalopathy.
    Changes in ingestive behavior V: Feline ischemic encephalopathy, brain hypoxia.
    I: Rabies, FSE, FIV.
    T: n.r.
    A: n.r.
    M: Hyperadrenocorticism, hyperthyroidism, lead poisoning, hepatic encephalopathy, uremic syndrome.
    I: n.r.
    N: Intracranial tumors: thalamus, ventromedial and posterolateral hypothalamus in the cat.
    D: n.r.
    Cognitive dysfunction, learning and memory deficits, dementia V: Feline ischemic encephalopathy, brain hypoxia.
    I: Distemper, FSE, mycotic meningoencephalitis, rabies, toxoplasmosis, neosporosis, Borna disease.
    T: Frontal lobe trauma.
    A: Hydrocephalus, hydrosyringomyelia, Chiari-like syndrome.
    M: Organic aciduria, lead poisoning, hepatic encephalopathy, uremic syndrome.
    I: n.r.
    N: Frontal lobe tumors.
    D: Age-related brain lesions, lysosomal storage diseases.
    Stereotypic and compulsive disorders V: Feline ischemic encephalopathy, brain hypoxia, polycythemia.
    I: Rabies, Aujeszky disease, granulomatous meningoencephalomyelitis, tetanus, FIV, erhlichiosis, necrotizing
    meningoencephalitis, necrotizing leukoencephalitis, protothecosis.
    T: Frontal lobe trauma, Reflex sympathetic dystrophy.
    A: Hydrocephalus, caudal occipital malformation syndrome, hydrosyringomyelia.
    M: Hypocalcemia, lead and thallium poisoning, Loperamide toxicity, hepatic encephalopathy, uremic syndrome, hypothyroidism, hyperadrenocorticism.
    I: Idiopathic ganglioradiculoneuritis, feline hyperesthesia syndrome, feline orofacial pain syndrome.
    N: Intracranial tumors: frontal lobes, basal nuclei (caudate nuclei).
    D: Spongy degeneration of the gray matter, axonal neuropathy, cauda equina syndrome.
    Non-specific Anxiety and Fear V: Feline ischemic encephalopathy, cerebrovascular accidents, brain hypoxia.
    I: Distemper, rabies, cryptococcosis, arthropod borne diseases, FSE, FIP, toxoplasmosis, neosporosis, Borna disease.
    T: Brain trauma, Reflex sympathetic dystrophy.
    A: Hydrocephalus, hydrosyringomyelia, Chiari-like syndrome.
    M: Hepatic encephalopathy, uremic syndrome, hypothyroidism, hypo- or hyperadrenocorticism, heavy metal poisoning.
    I: n.r.
    N: Intracranial tumors: frontal lobes, basal nuclei.
    D: n.r.
    Anomalies of sexual behavior V, I, T, A, M, I: n.r.
    N: Intracranial tumors: temporal lobes, limbic system, hypothalamus.
    D: Axonal neuropathy.

    In some cases the link between behavioural and neurological problems is unclear because of the lack of information. For instance, it has been found that the set of genes that contributes to narcolepsy seems to be involved also in anxiety disorder related to neurochemical system dysregulation [5]. Boundaries between behavioural conditions and medical differentials are likely to blur more rather than less as we learn more about genomic, cellular, and subcellular effects on common conditions. These changes should lead to better treatment but may also require a paradigm shift in how we view behavioural conditions and the mechanisms that contribute to them [15].

     
    CONCLUSION

    The boundary between neurological and behavioural disorders often is not clear, and they often coexist. As a matter of fact, many neurological conditions lead to behavioural changes, which can be the only sign and the first sign complained by the owners. Sometimes it is not possible to reach a diagnosis based only on neurology or on behavioural medicine. Finally, some behavioural problems can facilitate the onset or worsening of neurological conditions.
    A synergy between neurology and behavioural medicine would be beneficial for both of them, in the diagnostic procedure and in the treatment. Veterinarians of such disciplines should collaborate as much as possible.

     

    REFERENCES

    1. Overall KL. (2005). Veterinary behavioural medicine: a roadmap for the 21st century. The Veterinary Journal Proceedings of the Dogs Trust Meeting on Advances in Veterinary Behavioural Medicine London; 4th-7th November 2004: Veterinary behavioural medicine: a roadmap for the 21st century. 169(1), 130-143.
    2. Koehler W. (1962). The Koehler Method of Dog Training. Howell Book House, New York.
    3. Tuber DS, Hothersall D and Voith VL. (1974). Animal clinical psychology: a modest proposal. American Psychology. 29(10), 762-766.
    4. Mills DS, Heath SE and Harrington LJ. (1997). Proceedings of the First International Meeting on Veterinary Behavioural Medicine. UFAW, Potters Bar.
    5. Overall KL. (1997). Clinical Behavioral Medicine for Small Animals. Elsevier Mosby, St. Louis MO.
    6. Pageat P. (1998). Pathologie du Comportement du Chien, 2nd edition, Editions du Point Veterinaire, Maisons-Alfort.
    7. Donaldson D. (1998). Psychiatric Disorders with a Biochemical Basis. Parthenon, Carnforth, Lancs.
    8. Mills D. (2003). Medical paradigms for the study of problem behaviour: a critical review. Applied Animal Behaviour Science. 81(3), 265-277.
    9. Beata C, Bowen J, Fatjó J, Horwitz D, et al. (2009). Come scoprire e trattare l’ansia nel gatto. Veterinary Focus, Royal Canine, Special edition Chapter 2. 22-23.
    10. De Lahunta A and Glass E. (2010). Neuroanatomia e neurologia clinica veterinaria 3rd ed, Elsevier Masson, 7, 187-188.
    11. Bernardini M. (2010). Neurologia del cane e del gatto. 2nd ed, Poletto Editore.
    12. Fatjó J, Marin S, Manteca X and Palacio J. (1999). Animal behavior case of the month. Dominance aggression and pathologic aggression secondary to a brain tumor. Journal of the American Veterinary Medical Association. 215(9), 1254- 1256.
    13. Fatjò J and Bowen J. (2009). Medical and metabolic influenes on behavioural disorders. In Horwitz D.F, Mills D.S. BSAVA Manual of Canine and Feline Behavioural Medicine. 2nd Ed. BSAVA. 1-9.
    14. Seibert LM and Landsberg GM. (2008). Diagnosis and Management of Patients Presenting with Behavior Problems. In: Landsberg GM, Horwitz DF. Practical Applications and New Perspectives in Veterinary Behavior. The Veterinary Clinics of North America, Small Animal Practice 38(5), 937-950.
    15. Overall KL. (2003). Medical differential with potential behavioral manifestations. The Veterinary Clinics of North America. Small Animal Practice. 33(2), 213-229.
    16. Beaver BV. (2009). Canine Behavior of Sensory and Neural Origin. In: Canine Behavior: Insights and Answers, 2nd, Elsevier Health Sciences. 48-107.
    17. Overall KL. (2013). Manual of clinical behavioral medicine for dogs and cats. Elsevier Mosby, St. Louis MO.
    18. Falzone C and Lowrie M. (2011). Blindness and behavioural changes in the cat: common neurological causes. Journal of Feline Medicine and Surgery 13(11), 863-873.
    19. Greene CE, Vandevelde M and Braund K. (1976). Lissencephaly in 2 Lhapsa Apso dog. Journal of the American Veterinary Medical Association. 169(4), 405-410.
    20. Zaki FA. (1976). Lissencephaly in Lhasa Apso dogs. Journal of the American Veterinary Medical Association. 169(11), 1165-1168.
    21. Godbold JC Jr, Hawkins BJ and Woodward MG. (1979). Acute oral marijuana poisoning in the dog. Journal of American Veterinary Medical Association. 175(10), 1101-1102.
    22. Tyler DE, Lorenz MD, Blue JL, Munnell JF, et al. (1980). Disseminated protothecosis with central nervous system involvement in a dog. Journal of the American Veterinary Medical Association. 176(10), 987-993.
    23. Carmichael S, Griffiths IR and Harvey MJ. (1983). Familial cerebellar ataxia with hydrocephalus in bull mastiffs. Veterinary Record. 112(15), 354-358.
    24. Dubey JP. (1987). Toxoplasmosis. Veterinary Clinics of North America Practice. 17(1), 389-404.
    25. Ferguson DC and Hoenig M. (1990). Hypethyroidism in the cat. Feline Practice. 18, 10.
    26. Egberink HF. (1990). Aujeszky’s disease in dogs and cats. Tijdschr Diergeneeskd. 115(8), 349-353.
    27. Chrisman CL. (1991). Problems in small animal neurology. 2nd Edition Lea&Febinger editors.
    28. Podell M, Oglesbee M, Mathes L, Krakowka S, et al. (1993). AIDS-associated encephalopathy with experimental feline immunodeficiency virus infection. Journal of Acquired Immuedeficiency Sindromes. 6 (7), 758-771.
    29. Jaggy A, Oliver JE, Ferguson DC, Mahaffey EA, et al. (1994). Neurological manifestations of hypothyroidism: a retrospective study of 29 dogs. Journal of Veterinary Internal Medicine. 8(5), 328-336.
    30. Taboada J and Dimski DS. (1995). Hepatic encephalopathy: clinical signs, pathogenesis, and treatment. Veterinary Clinic of North American Small Animal Practice. 25(2), 337-355.
    31. Summers BA, Cummings JF and de Lahunta A. (1995). Veterinary neuropathology, St Louise, Mosby, 242-244.
    32. Dodman NH, Knowles KE, Shuster L, Moon-Fanelli AA, et al. (1996). Behavioral changes associated with suspected complex partial seizures in bull terriers. Journal of the American Veterinaty Medical Association. 208(5), 688-691.
    33. Phillips TR, Prospero-Garcia O, Wheeler DW, Wagaman PC, et al. (1996). Neurologic dysfuncions caused by a molecular clone of feline immunodeficiency virus, FIV-PPR. Journal of Neurovirology. 2(6), 388-396.
    34. Harrington ML, Bagley RS and Moore MP. (1996). Hydrocephalus. The Veterinary Clinics of North America, Small Animal Practice. 26(4), 843-856.
    35. Smith MO, Wenger DA, Hill SL and Matthews J. (1996). Fucosidosis in a family of American-bred English Springer Spaniels. Journal of American Veterinary Medical Association. 209 (12), 2088-2090.
    36. Odendaal JS. (1997). A diagnostic classification of problem behaviour in dogs and cats. The Veterinary Clinics of North America. Small Animal Practice. 27 (3), 427-443.
    37. Jull BA, Merryman JI, Thomas WB and McArthur A. (1997).Necrotizing encephalitis in a Yorkshire terrier. Journal of American Veterinary Medical Associations. 211(8), 1005-1007.
    38. LaBarre A and Coyne BE. (1999). Reflex sympathetic dystrofhy in a dog. Journal of the American Animal Hospital Association. 35(3), 229-231.
    39. Cantile C, Chianini F, Arispici M and Fatzer R. (2011). Necrotizing meningoencephalitis associated with cortical hippocampal hamartia in a Pekingese dog, Veterinary Patholology. 38(1), 119-122.
    40. Cantile C, Baroni M and Arispici M. (1999). A case of narcolepsy- cataplexy associated with distemper encephalitis. Zentralbl Veterinarmed A. 46(5), 301-308.
    41. Gandini G, Steffen F and Jaggy A. (1999). Encefalopatia epatica secondaria a shunt porto sistemico congenito nel cane: apetti clinici, neurologici, laboratoristici e postoperatori in 17 cani. Veterinaria. 13(3), 25-37.
    42. Uchida K, Hasegawa T, Ikeda M, Yamaguchi R, et al. (1999). Detection of an autoantibody from Pug dogs with necrotizing encephalitis (Pug dog encephalitis). Veterinary Patholology. 36(4), 301-307.
    43. Greene CE. (2012). Rabies and Other Lissavirus Infections. In Green CE.: Infectious diseases of the dog and cat, 4th edition, Philadelphia: WB Saunders Co. 179-197.
    44. Vandevelde MZ, Tipold A, Schatzberg SJ and Green EC. (2012). Neurologic disease of suspected infectious origin and prion disease. In: Green C.E., Infectious diseases of the dog and cat, 4th ed., Philadelphia: WB Saunders Co. 853-864
    45. Fatzer R, Gandini G, Jaggy A, Doherr M, et al. (2000). Necrosis of hippocampus and piriform lobe in 38 domestic cats with seizures: a retrospective study on clinical and pathologic findings. Journal of Veterinary Internal Medicine. 14(1), 100- 104.
    46. Sellon RK and Hartmann K. (2012). Feline Immunodeficiency virus infections. In: Green CE, Infectious diseases of the dog and cat, 4th ed., Philadelphia: WB Saunders Co. 36-149.
    47. Webb AA, Taylor S and Muir GD. (2008). Steroid-responsive meningitis-arteritis in dogs with noninfectious, nonerosive, idiopathic, immune-mediated polyarthritis. Journal of Veterinary Internal Medicine. 16 (3), 269-273.
    48. Abramson CJ, Platt SR, Jakobs C, Verhoeven NM, et al. (2003). L-2-Hydroxyglutaric aciduria in Staffordshire Bull Terriers. Journal of Veterinary Internal Medicine. 17 (4), 551-556.
    49. Fogelman V, Fischman HR, Horman JT and Grigor JK. (1993). Epidemiologic and clinical characteristics of rabies in cats. Journal of the American Veterinary Medical Association. 202 (11), 1829-1833.
    50. Barfield DM, Pegrum SA, Snow D and Malik R. (2007). Pupillary dilation, tachycardia and abnormal behaviour in a young cat. Diagnosis: cocaine intoxication. Journal of Feline Medicine and Surgery. 9(4), 65-270.
    51. Behr S and Cauzinille L. (2006). Aseptic suppurative meningitis in juvenile boxer dogs: retrospective study of 12 cases. Journal of the American Animal Hospital Association. 42 (4), 277-282.
    52. Collins NM, Keen JA, Barakzai SZ, Mayhew IG, et al. (2006). Suspected complex regional pain syndrome in two horses. Journal of Veterinary Internal Medicine, 20(4), 1014-1017.
    53. Salvadori C, Lossi L, Arispici M and Cantile C. (2007). Spongiform neurodegenerative disease in a Persian kitten. Journal of Feline Medicine & Surgery. 9(3), 242-245.
    54. Wrzosek M, Konar M, Vandevelde M and Oevermann A. (2009). Cerebral extension of steroid-responsive meningitis arteritis in a boxer. Journal of Small Animal Practice. 50(6), 319.
    55. Carrera I, Dennis R, Mellor DJ, Penderis J, et al. (2009). Use of magnetic resonance imaging for morphometric analysis of the caudal cranial fossa in Cavalier King Charles Spaniels. American Journal of Veterinary Research. 70(3), 340-345.
    56. Tipold A and Schatzberg SJ. (2010). An update on steroid responsive meningitis-arteritis. Journal of Small Animal Practice. 51(3), 150-154.
    57. Rusbridge C, Heath S, Gunn-Moore DA, Knowler SP, et al. (2010). Feline orofacial pain syndrome (FOPS): a retrospective study of 113 cases. Journal of Feline Medicine & Surgery, 12(6), 498-508.
    58. Gunn-Moore DA and Reed N. (2011). CNS disease in the cat: current knowledge of infectious causes. Journal of Feline Medicine and Surgery. 13 (11), 824-836.
    59. Nakamoto Y, Yamato O, Uchida K, Nibe K, et al. (2011). Neuronal ceroid-lipofuscinosis in longhaired Chihuahuas: clinical, pathologic, and MRI findings. Journal of American Animal Hospital Association. 47(4), 64-70.
    60. Davies ES, Volk HA, Behr S, Summers B, et al. (2012). Porencephaly and hydranencephaly in six dogs. Veterinary Record. 170(7), 179.
    61. Rutherford L, Wessmann A, Rusbridge C, McGonnell IM, et al. (2012). 2012 Questionnaire-based behaviour analysis of Cavalier King Charles spaniels with neuropathic pain due to Chiari-like malformation and syringomyelia. Veterinary Journal. 194 (3), 294-298.
    62. Zarelli M, Shiel R, Gallagher B, Skelly C, et al. (2012). Imaging diagnosis: CT findings in a dog with intracranial hemorrhage secondary to angiostrongylosis. Veterinary Radiology & Ultrasound. 53 (4), 420-423.
    63. De Risio L, Brown R, Tennant B, Sparkes A, et al. (2012). Slowly progressive lymphohistiocytic meningoencephalomyelitis in 21 adult cats presenting with peculiar neurological signs. Journal of Feline Medicine and Surgery. 14(4), 250-256.
    64. Vanhaesebrouck AE, Posch B, Baker S, Plessas IN, et al. (2012). Temporal lobe epilepsy in a cat with a pyriform lobe oligodendroglioma and hippocampal necrosis. Journal of Feline Medicine and Surgery. 14(12), 932-937.
    65. Cantile C, Arispici M, Modenato M and Fatzer R. (1997). Hydroencephalus with periventricular encephalitis in the dog. Zentralbl Veterinarmed A. 44(9-10), 595-601.
    66. Gunn-Moore DA. (2011). Cognitive dysfunction in cats: clinical assessment and management. Topics in Companion Animal Medicine. 26(1), 17-24.
    67. Salvadori C, Gandini G, Ballarini A and Cantile C. (2008). Protothecal granulomatous meningoencephalitis in a dog. Journal of Small Animal Practice. 49(10), 531-535.

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